The influence of antidepressant therapy on the level of brain-derived neurotrophic factor in the blood serum of patients with melancholic depression: a pilot study

Background. The study of pathogenetic mechanisms of depression, as well as the prediction and implementation of princi-ples of effective therapy for this disease are of primary importance. Brain-derived neurotrophic factor (BDNF) is considered to be one of the key components of pathogenetic mechanisms of depressive disorders. Objective: to determine the BDNF level in the blood serum of patients with melancholic depression under antidepressant therapy. Materials. The sample included patients diagnosed with the current episode of mild or moderate depression (F31.3). According to ICD-10 and DSM-5 criteria, this con-dition is classified as melancholic depression in the structure of bipolar II disorder. The main group (n=54) was predominated by female patients (63% vs 37%). The mean age of patients was 26 years; IQR [22; 37]. The control group consisted of 11 healthy volunteers without a diagnosis of mental disorder, who matched the patients in the main group by gender and age. 21 patients of 54 were examined for BDNF concentration in the blood serum. Methods: clinical-psychopathological, clinical-dynamic, laboratory, mathematical statis-tics. Clinical-psychopathological examination was performed twice: at baseline and during antidepressant therapy (venlafaxine 75-150 mg/day, lamotrigine 125-150 mg/day) by days 28-30. The severity of de-pression and anxiety was determined using the Hamilton clinical scales. The concentration of BDNF in the serum was deter-mined by ELISA using a reagent kit for quantitative determination (96 determinations) of BDNF by enzyme immunoassay (human brain-derived neurotrophic factor, BDNF, ELISA Kit, Cusabio Technology LLC, US). Results. Despite the revealed improvement in the clinical status of the patients, the normalization of the BDNF level in the blood serum was not established 30 days after the start of therapy when comparing the patients’ parameters at baseline (n=21) and after the treatment (n=8): Me 15.2; IQR [8.2; 34.1] ng/ml serum vs Me 13.35; IQR [9.73; 43.1] ng/ml of serum (p> 0.05), as well as compared with the BDNF level in healthy controls: Me 19.84 (IQR [13.47; 26.32]; n=11) ng/ml. At the same time, a statistically significant (p<0.05) lower concentration of BDNF in the blood serum was found when compared with the control indices (healthy volun-teers; n=11): Me 19.84; IQR [13.47; 26.32] ng/ml of serum. Discussion. In patients with melancholic depression, antidepres-sant therapy had no effect on the BDNF concentration in the blood serum, since the BDNF levels in the blood serum at baseline and after antidepressant therapy were approximately the same, but were statistically significantly lower relative to the indices in healthy volunteers of the control group. Conclusion. The lack of dynamics in the BDNF concentration in the blood serum of patients with melancholic depression at baseline and after antidepressant therapy is explained by dysfunction of the blood-brain barrier. We hypothesize that oxidative stress, dysfunction of the transport protein P-glycoprotein, impaired cortisol metabolism and effect of vascular endothelial growth factor (VEGF) on the secretion of BDNF from brain cells are involved in this patho-logical process.